Extracranial Arterial Dissection
Anticoagulation Is the Treatment of Choice: For
Section Editors: Geoffrey A. Donnan MD, FRACP Stephen M. Davis MD, FRACP
Anticoagulant therapy has been advocated consistently as the treatment of choice for cervical arterial dissection in numerous published studies and reviews,1 but there is little evidence-based data to justify this assumption. Although dissection of the cervical arteries has long been established as a cause of ischemic and hemorrhagic stroke, the major obstacle to planning therapeutic studies has been the perception that this is a relatively rare phenomenon. However, rapid developments in accurate noninvasive imaging have shown cervical arterial dissection as a common, if not the most common, cause of ischemic stroke in persons <50 years of age. This has raised for the first time the realistic concept of a therapeutic trial of anticoagulants versus antiplatelet treatment. A recent Cochrane review2 cited a figure of 1000 patients in each therapeutic arm, and similar figures were calculated from the only prospective study published to date.3
Arterial dissection can theoretically cause ischemic stroke either by embolism from the site of the intimal tear, or hemodynamically from luminal obstruction. Available evidence strongly favors artery-to-artery embolism as the most common cause, and the pattern of cerebral infarction in stroke from dissection is typical of that seen in other types of cerebral embolism.4 Even more interesting, microemboli have not only been detected by transcranial Doppler in acute cervical arterial dissections, but they also correlate with the presence of stroke in patients with traumatic and “spontaneous” dissections.5
All these factors intuitively favor the use of anticoagulant therapy, at least in the immediate poststroke phase, to minimize distal embolism from the site of the tear, but accumulating data of the underlying pathology of dissection indicate that its mechanics are more complex than previously believed. Carotid endarterectomy in patients with acute dissection may reveal previously healed asymptomatic dissections in the same vessel.6 Also, neurovascular imaging sometimes shows silent redissection in the same cervical artery in patients receiving anticoagulants for previous dissection, raising the possibility that these drugs encourage further dissection of the vessel wall,7 though most observers believe this is a rare event and should not discourage anticoagulant therapy.
However, these findings do raise another caveat for the use of heparin or warfarin in acute dissection; the occurrence of unsuspected subarachnoid hemorrhage from intracranial involvement, which is probably much more frequent than generally believed. Dissections may track silently along the course of the extracranial part of the cervical artery, only to declare themselves as subarachnoid hemorrhage when they arrive at the intracranial portion. The structure of the intracranial cervical vessels differs from that of the extracranial arteries. Once they pierce the dura, there is anatomical attenuation and weakening of the media, which facilitates rupture of the vessel wall, allowing blood to track right through to the subadventitia, and so into the subarachnoid space.8 Clearly, when there is the slightest doubt, lumbar puncture should be performed to exclude dissection before administering anticoagulant therapy, especially in patients where headache is a major symptom.
In spite of these reservations, most neurologists use anticoagulants as the first line of treatment in acute cervical arterial dissection. In a recent nationwide survey of Canadian neurologists, anticoagulant therapy was the treatment of choice for 81% of physicians, though admittedly on empirical grounds only.9 The usual regimen is to follow immediate heparin therapy with longer-term warfarin for 3 months and then decide on further management depending on vascular imaging. Enhanced magnetic resonance angiography is now almost as accurate as catheter angiography, but without the complications of the invasive procedure, and computerized tomographic angiography is proving even better. Angiography should be performed urgently because imaging abnormalities are often very transient. Doppler ultrasound is in general disappointing, even for screening purposes, because although it is sensitive to flow changes, it has limited anatomical range in the neck and limited ability to show minor but critical damage to the vessel wall, such as intimal flaps, minor wall irregularities, or “false” aneurysms.
In the presence of these structural abnormalities, it is customary to continue anticoagulant therapy for another 3 months even in the absence of symptoms, but if the vessel has returned to normal, as in most cases, aspirin treatment is usually given for another 3 months. In the internal carotid artery, dissections occur 1 to 2 cm more distally to the bulb than in atherosclerosis, where the wall changes from an elastic to a muscular structure, which is an ideal location for stenting should symptoms continue in spite of adequate anticoagulation.10
All these uncertainties would be dispelled if a randomized controlled trial could be undertaken. Two separate and independent studies have arrived at similar numbers for such a trial, involving a total of ≈2000 patients.2,3 This number would be large but not unwieldy using present information technology. The time for this trial has arrived.
- Received April 1, 2005.
- Accepted April 6, 2005.
Lyrer P, Engelter S. Antithrombotic drugs for carotid artery dissection (Cochrane Review) Oxford, UK. Cochrane Library;. 2002, Issue 1.
Beletsky V, Nadareishvili Z, Lynch J, Shuaib A, Woolfenden A, Norris JW; for the Canadian Stroke Consortium. Cervical arterial dissection: time for a therapeutic trial? Stroke. 2003; 34: 2856–2860.
Lucas C, Moulin T, Deplanque D, Tatu L, Chavot D; and the DONALD investigators. Stroke. 1998; 29: 2646–2648.
Srinivasan J, Newell DW, Sturznegger M, Mayberg MR, Winn HR. Transcranial Doppler in the evaluation of internal carotid artery dissection. Stroke. 1996; 27: 1226–1230.
Goldstein LB, Gray L, Hulette CM. Stroke due to recurrent ipsilateral carotid artery dissection in a young adult. Stroke. 1995; 26: 480–483.
Siddiqi J, Levy C, Amarenco P, Bousser M-G. Ipsilateral internal carotid artery redissection on anticoagulants. Stroke. 1995; 26: 1302–1303.
Schievink WI, Mokri B, Piepgras DG. Spontaneous dissections of cervicocephalic arteries in chidhood and adolescence. Neurology. 1994; 44: 1607–1612.
Hill M, Granger H, Perry JR. Extracranial cervical arterial dissection. Stroke. 2000; 31: 791.